Abstract
Early developmental conditions are known to have life-long effects on an individual’s behavior, physiology and fitness. In altricial birds, a majority of these conditions, such as the number of siblings and the amount of food provisioned, are controlled by the parents. This opens up the potential for parents to adjust the behavior and physiology of their offspring according to local post-natal circumstances. However, the mechanisms underlying such intergenerational regulation remain largely unknown. A mechanism often proposed to possibly explain how parental effects mediate consistent phenotypic change is DNA methylation. To investigate whether early life effects on offspring phenotypes are mediated by DNA methylation, we cross-fostered great tit (Parus major) nestlings and manipulated their brood size in a natural study population. We assessed genome-wide DNA methylation levels of CpG sites in erythrocyte DNA, using Reduced Representation Bisulfite Sequencing (RRBS). By comparing DNA methylation levels between biological siblings raised in enlarged and reduced broods and between biological siblings of control broods, we assessed which CpG sites were differentially methylated due to brood size. We found 32 differentially methylated sites (DMS) between siblings from enlarged and reduced broods, a larger number than in the comparison between siblings from control broods. A considerable number of these DMS were located in or near genes involved in development, growth, metabolism, behavior and cognition. Since the biological functions of these genes line up with previously found effects of brood size and food availability, it is likely that the nestlings in the enlarged broods suffered from nutritional stress. We therefore conclude that early life stress might directly affect epigenetic regulation of genes related to early life conditions. Future studies should link such experimentally induced DNA methylation changes to expression of phenotypic traits and assess whether these effects affect parental fitness to determine if such changes are also adaptive.
Highlights
Developmental phenotypic plasticity can be defined as irreversible changes in the phenotype resulting from environmentally introduced alterations in development (Forsman, 2015)
The mechanisms underlying intergenerational regulation of developmental phenotypic plasticity in birds remain largely unknown, but recent studies indicate a role for DNA methylation (Bentz et al, 2016; Sheldon et al, 2018)
We found more CpG sites in red blood cells to be differentially methylated between biological siblingpairs raised in experimentally enlarged and reduced broods, than between siblings raised in partially cross-fostered control broods with unchanged brood size
Summary
Developmental phenotypic plasticity can be defined as irreversible changes in the phenotype resulting from environmentally introduced alterations in development (Forsman, 2015) These changes can occur through parental effects, which occur when the parental environment or phenotype affects that of their offspring. A likely reason why parents adjust their offspring’s phenotype is to maximize parental fitness (Reddon, 2012), by transferring information about the current environment to their offspring and subsequently shape their offspring’s phenotype to match the environmental conditions. If these conditions remain stable, this might increase their offspring’s reproduction or survival (Champagne et al, 2003; Dantzer et al, 2013)
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call